In humans, IKUR - is an atrial-specific, ultra-rapid, delayed rectifier K+ current that is increased by (beta-adrenergic stimulation. Although the cloned K+ channel, Kv1.5 is the principal molecular correlate of IKUR, our preliminary data suggest that co-assembly of other factors or proteins is required to recapitulate the native current and its modulation by protein kinase A (PKA). We will test the hypothesis that Kv1.5 is part of a multi-protein complex that includes an A Kinase Anchoring Protein (AKAP) that targets PKA to the channel. Using electrophysiologic techniques, the role of AKAP co-expression with Kvl.5 to enable the PKA response will be examined. In addition, I will test the hypothesis that an auxiliary K+ channel beta subunit can function as an AKAP. Finally, I will investigate what molecules co- assemble with Kv1.5 in human atria. Given the atrial specificity of this K+ current in humans, novel strategies to treat atrial-based arrhythmias such as atrial fibrillation may result.